Nutrition Flashcards
50s M w/ RYGB 10yo w. fatigue. PE ataxic gait. Labs microcytic, hypochromic anemia, and mild leukopenia and neutropenia. deficiency?
A. Zinc
B. Vitamin B12
C. Iron
D. Copper
- copper deficiency -
- microcytic, hypochromic anemia
- leukopenia & neutropenia
- neurologic disturbances - particularly ataxic gait
- Prevalence-10-20% post-RYGB
- zinc deficiency
- change in or absence of taste
- skin lesions
- alopecia, and
- delayed wound healing
- not associated with neurologic abnormalities
50s M, RYGB 18mo ago, here for management of obesity and type 2 diabetes. Doing well until a few months ago when he developed hair loss, dysgeusia, loss of appetite, and diarrhea. He has been followed by his bariatric surgery care team and appears to be compliant with the dietary plan and recommended supplements. Deficiency?
A. Vitamin B12
B. Zinc
C. Vitamin K
D. Copper
- Although several nutrient deficiencies can result in hair loss, the specific combination of symptoms found in this patient are most consistent with zinc deficiency.
- Zinc homeostasis depends on intake, small intestinal absorption, and intestinal losses.
- After RYGB, dietary nutrient intake is decreased due to a reduction in gastric capacity.
- Furthermore, zinc absorption mainly takes place in the duodenum and proximal jejunum which are bypassed in RYGB. Therefore, zinc deficiency can occur despite supplementation and can be seen in up to 40% of patients after RYGB.
- Vitamin B12 deficiency can lead to anemia, neuropathy, vision loss, paresthesia, muscle weakness, cognitive issues, glossitis, and weight loss.
- Vitamin K deficiency can result in coagulopathy which can lead to bruising or bleeding. In RYGB patients, vitamin K deficiency may be associated with deficiencies of other fat-soluble vitamins.
- Patients with copper deficiency can develop neuropathy, skin changes, increased muscle tone or spasticity, progressive difficulty walking, anemia, and neutropenia.
A 22-year-old woman is referred to you as a third opinion to address chronic, meal-related nausea, bloating, abdominal pain, and irregular bowel habits with more constipation than diarrhea. She reports a prior diagnosis of IBS-C. She tells you her symptoms have progressively worsened over the past 24 months resulting in a 15-20-lb weight loss. Her body mass index is 18. Previous workup with laboratory tests, endoscopy with biopsies, and abdominal/pelvic CT scan was negative. Allergy and motility testing have been unremarkable other than equivocal testing for anorectal manometry. Osmotic laxatives and physical therapy have been ineffective. She has been progressively eliminating foods that trigger her symptoms and is currently taking a very limited diet. What is the next best step in helping this patient?
A. Begin therapy with senna to address her constipation.
B. Refer the patient back to physical therapy to address incompletely treated dyssynergic defecation.
C. Begin the low FODMAP diet.
D. Consider an eating disorder and solicit the aid of a GI dietitian and psychiatrist.
It is clear that this patient has more than the usual functional dyspepsia or irritable bowel syndrome. Her workup has been comprehensive and unrevealing, and she has failed multiple over-the-counter and prescription medications. While it is reasonable to consider rare causes of these symptoms, gastroenterologists should be suspicious for an eating disorder in such a patient. Eating disorders are surprisingly common in patients with GI complaints, and the majority of patients with eating disorders report GI symptoms. Malnutrition and low BMI have been independently associated with GI symptoms and diagnoses, particularly motility disorders such as gastroparesis and constipation. In particular, Avoidant Restrictive Food Intake Disorder (ARFID) should be considered in this patient taking a highly restricted diet in association with significant weight loss and interference with her daily activities. ARFID patients may require enteral feeding for nutritional support. Evidence of ARFID has been reported in 20% of adult patients with functional GI disorders. Treatment of ARFID patients requires a team-based multidisciplinary approach to establish and help the patient to understand the diagnosis as well as provide effective treatment. Restrictive elimination diets like the low FODMAP diet are not appropriate if there are concerns for ARFID. The patient has already tried osmotic laxatives and physical therapy so there is little value in trying treatments directed at constipation alone. Also, while PEG can be helpful for stool frequency and consistency, it would not be expected to help with this patient’s other GI complaints of nausea, pain, or bloating.
A 45-year-old man with a longstanding history of Crohn’s disease and prior intestinal resections presents with high ostomy output. He has a history of total colectomy and 2 prior small bowel resections leaving him with 90 cm of small bowel to an end ostomy. Due to a weight loss of 50 lb, the patient is started on home parenteral nutrition (PN). The PN includes a soy-lipid formulation dosed at 1 g/kg of actual body weight. Six months after the initiation of PN, routine laboratory assessment demonstrates elevations in: AST 40 U/L (normal: 0-35 U/L), ALT 111 U/L (normal: 0-35 U/L), alkaline phosphatase 339 U/L (normal: 36-92 U/L), and total bilirubin 2.4 mg/dL (normal: 0.3-1.2 mg/dL). Liver biopsy demonstrated normal liver architecture and no evidence of fibrosis. The liver parenchyma demonstrated hepatocellular and canalicular cholestasis [figure]. Which of the following interventions is the appropriate next step in the management of the cholestatic liver disease?
A. Reduced amount of administered lipid
B. Exogenous carnitine supplementation
C. Transition to a fish oil lipid formulation
D. Trial of oral antibiotics
- Although more common in neonates, cholestasis as a result of PN is well described in adult patients. Intestinal failure-associated liver disease (IFALD) can present on a spectrum from cholestasis to steatohepatitis, progressing to cirrhosis.
- A number of etiologies have been described contributing to IFALD including short bowel syndrome (SBS), lipid source and amount, altered bile acid signaling, small bowel bacterial overgrowth, and vitamin deficiencies.
- A prior clinical trial failed to demonstrate improvement in liver function studies with intravenous carnitine supplementation. Although IFALD has been associated with total lipid dose, the phytosterol content of soy-based lipid emulsions has been associated with cholestasis and hepatic complications.
- Therefore, pure fish oil lipid emulsions and mixed lipid emulsions containing fish oil have been described to improve cholestatic liver injury in both children and adults.
36M ed w/ 4-wk history of intractable vomiting and rapid weight loss 7 months after RYGB. He appears dehydrated and mildly confused. He is given a bolus of normal saline and then is maintained on D5 ½ NS and admitted to the hospital for further evaluation and management. By the time he reaches his hospital room, he has become more confused and ataxic with evidence of nystagmus and right lateral ophthalmoparesis. He denied a history of alcohol abuse and a toxicology screen was negative. An upper endoscopy shows normal postoperative findings and a brain MRI is normal. Which one of the following is most likely responsible for his deterioration?
A. Thiamine deficiency
B. Copper deficiency
C. Vitamin B12 deficiency
D. Essential fatty acid deficiency
- Wernicke’s encephalopathy (WE) is due to dysfunction of central gray structures surrounding the third and fourth ventricles caused by thiamine deficiency. Occurring both in patients with and without an alcohol use disorder, it is a rare but increasingly recognized cause of encephalopathy in the bariatric surgery patient who classically presents with protracted vomiting.
- WE is characterized by the triad of confusion, ataxia, and ophthalmoplegia. Prompt treatment with intravenous thiamine can reverse WE, although some symptoms may be permanent if not corrected quickly.
- WE may be iatrogenically precipitated by glucose loading in patients with unsuspected thiamine deficiency. To avoid this complication, it has become standard practice in emergency departments to administer thiamine prior to or along with glucose infusion, particularly in those who are at risk for thiamine deficiency.
A 65-year-old woman with a history of hypertension, smoking, and remote history of cervical cancer treated with definitive radiation therapy presented to the emergency department with abdominal pain and distension. She was diagnosed with a small bowel obstruction in the terminal ileum on cross-sectional imaging. Prior to presentation, the patient reported a 6-month history of weight loss and intermittent obstructive symptoms. The patient undergoes surgical ileocecectomy with resection of 70 cm of terminal ileum. Due to the history of radiation, a proximal loop ileostomy was created. Three weeks following discharge, the patient presented to the hospital with an acute kidney injury and ostomy output of 2 liters per day despite management with loperamide, proton pump inhibitors, and initiation of oral rehydration solution. What is the best approach to management?
A. Initiation of teduglutide
B. Initiation of parenteral nutrition
C. Surgical takedown of diverting ostomy
D. Initiation of elemental enteral nutrition
Although teduglutide would be expected to reduce ostomy output, teduglutide is only indicated for individuals already requiring parenteral support. This patient has evidence of high ostomy output despite initiation of appropriate therapies to include bowel slowing agents, proton pump inhibitors, and oral rehydration solution. Initiation of parenteral support is required to account for the intestinal losses of water and electrolytes. Although surgical takedown of the diverting ostomy will be required in the long term, early ostomy takedown places the patient at risk for intra-abdominal infectious complications. Hyperosmolar elemental enteral nutrition formulas place the patient at risk for higher ostomy output by acting as an osmotic agent and drawing water into the intestinal lumen.
You are asked to consult on a 32-year-old woman admitted with progressive asymmetric weakness and severe normocytic anemia. She denies any bleeding, and she is guaiac negative. Past surgical history includes a Roux-en-Y gastric bypass 20 years ago. Otherwise, she has no past medical history. She has no known family history. She denies smoking, alcohol, or substance abuse. She takes no medications. Vitals are normal. On exam, you appreciate ataxia, dysarthria, nystagmus, diminished knee and ankle deep tendon reflexes, and loss of proprioception and vibratory sensation. Remainder of the physical exam is unremarkable with preserved mentation, normal affect, benign abdominal exam, and no evidence of skin rash or glossitis.
Pertinent laboratory tests show the following:
Hemoglobin 5.8 g/dL (normal: 12-16 g/dL)
Hematocrit 13.4% (normal: 35%-45%)
MCV 80.5 fL (normal: 80-100 fL)
Platelets 167,000/µL (normal: 150,000-350,000/µL)
Reticulocyte count 8.1% (normal: 0.5%-1.5% of erythrocytes)
Serum iron 140 µg/dL (normal: 60-160 µg/dL)
Haptoglobin 2 mg/dL (normal: 50-150 mg/dL)
LDH 1870 IU/L (normal: 0-250 IU/L)
Total bilirubin 1.7 mg/dL (normal: 0.2-1.2 mg/dL)
The remaining renal, hepatic, and coagulation tests are normal. Additional extensive laboratory and diagnostic work-up excluded a rheumatologic or neurologic condition. What vitamin deficiency does the patient most likely have?
A. Vitamin B12
B. Vitamin B3 (niacin)
C. Vitamin A
D. Vitamin E
- This patient has hemolytic anemia and neurologic deficits from vitamin E deficiency due to inadequate small intestinal absorption of fat-soluble vitamins in the setting of a previous gastric bypass
- Vitamin E (α-tocopherol) is an important fat-soluble nutrient that serves as an immunomodulator, an antioxidant, and antiplatelet.
- Deficiency is rare and is defined as <0.5 mg/dL. It should be suspected in medical conditions where fat malabsorption occurs such as:
- (1) small bowel resection and
- (2) small bowel malabsorption (i.e., cystic fibrosis, pancreatic insufficiency).
- Clinical features of deficiency can include progressive neuromuscular deficits, hemolytic anemia, blindness, and dementia.
- Vitamin B12 deficiency can present with similar manifestations including neuromuscular deficits and hemolytic anemia, although several distinguishing clinical features exist.
- First, the anemia in B12 deficiency is usually macrocytic with an MCV greater than 100 and this patient has normocytic anemia.
- Secondly, neuropsychiatric symptoms seen with B12 deficiency such as personality changes and psychosis are usually absent in vitamin E deficiency, and this patient had normal affect and mentation.
- Thirdly, findings suggesting spinocerebellar involvement tend to be more prominent with vitamin E deficiency including dysarthria, nystagmus, and tremor which were notable in this patient.
- In contrast, neurologic deficits in B12 deficiency mostly result from subacute combined degeneration of the spinal cord; therefore, patients with B12 deficiency may have more prominent upper motor neuron signs (i.e., spastic paraparesis, Babinski’s).
- Niacin deficiency can result in pellagra, dementia, diarrhea, and dermatitis.
- Vitamin A deficiency can result in night blindness, rashes, poor bone growth, and an impaired immune system.
A 78-year-old woman with a history of coronary artery disease, hypertension, and vascular dementia is brought to the hospital by her family after awakening with a new-onset, left-sided hemiplegia. The patient is found to have a large infarct in the territory of the right middle cerebral artery. On hospital day 2, the gastroenterology service is consulted for recommendations on nutritional support. The patient has a BMI of 17.8 kg/m2 and on exam has evidence of bilateral temporal muscle wasting. Due to alterations in consciousness, she is unable to participate in a bedside swallow evaluation. What is the most appropriate step in management of this patient?
A. Initiation of parenteral nutrition
B. Placement of a gastrostomy tube
C. Initiation of enteral feedings via nasogastric tube
D. Defer nutrition support until hospital day 7
- Although the patient has clinical signs of malnutrition with a low BMI and evidence of muscle wasting, early parenteral support is not indicated without evidence of intestinal failure or contraindications to enteral nutrition support. The FOOD trial demonstrated reductions in death and poor outcomes with the initiation of early enteral support in the setting of stroke. Early feeding via gastrostomy tube, when compared to nasogastric tube was associated with an absolute increased risk of death and survival with poor outcomes. Therefore, early initiation of enteral nutrition support is recommended via nasogastric tube following cerebrovascular accident with placement of a percutaneous endoscopic gastrostomy tube reserved for individuals intolerant of nasogastric feeding or following a 1-2 week trial of nasogastric feedings and failure to achieve adequate advancement of oral diet.
Mediterranean diet?
POUNDS LOST Study?
- Although the 2013 AHA/ACC/TOS guideline for the management of overweight and obese adults recommends that any diet can be associated with weight loss, all of the cardiometabolic benefits of weight loss may not be seen in the weight maintenance phase. However, in the absence of weight loss, a 5-year study found that the Mediterranean diet was associated with a reduction in a composite of acute myocardial infarction, stroke, or death from cardiovascular causes.
- In the POUNDS LOST study investigating the effects of different macronutrient diets, there was no correlation with the macronutrient content, but a direct correlation with the number of visits with the weight loss team and weight loss.
